CLINICAL STUDIES
Effect of angiotensin-converting enzyme inhibition and angiotensin II type 1 receptor antagonism on postprandial endothelial function
Hanneke W. Wilmink, MD*,
Jan D. Banga, MD, PhD*,
Michel Hijmering, MD ,
Willem D. Erkelens, MD, PhD*,
Erik S. G. Stroes, MD, PhD and
Ton J. Rabelink, MD, PhD
* Division of Internal Medicine, University Hospital Utrecht, Utrecht, The Netherlands
Division of Nephrology and Hypertension, University Hospital Utrecht, Utrecht, The Netherlands
Manuscript received September 11, 1998;
revised manuscript received February 16, 1999,
accepted March 19, 1999.
Reprint requests and correspondence: Dr. T. J. Rabelink, Department of Nephrology and Vascular Medicine, F 03.226, University Hospital Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands
T.Rabelink{at}DIGD.AZU.NL
OBJECTIVES
The purpose of this study was to determine whether endothelial dysfunction as a consequence of direct postprandial lipid response might be favorably influenced by angiotensin-converting enzyme inhibitors or angiotensin AT1 receptor antagonists.
BACKGROUND
Postprandial triglyceride-rich lipoproteins cause endothelial dysfunction. Angiotensin-converting enzyme inhibitors have been shown to improve vascular reactivity. For angiotensin II type 1 receptor antagonists this effect is as yet uncertain.
METHODS
A randomized, double-blind, placebo-controlled crossover study in 30 healthy volunteers, aged 18 to 33 years, evaluated the effect of quinapril (40 mg daily for two weeks) and losartan (50 mg daily for two weeks) on basal as well as postprandial endothelial function measured noninvasively as percentage diameter change in the brachial artery after reactive hyperemia. Endothelium-independent dilation was measured after nitroglycerine spray sublingual.
RESULTS
An acute oral fat load impaired endothelial function. Flow-mediated vasodilation (FMD) decreased from a median of 6.2% to 4.2% (p < 0.05). There was no significant difference in preprandial endothelial function after two weeks of treatment with either quinapril or losartan compared with placebo in these healthy volunteers. Both quinapril (FMD 6.4% to 6.3%) and losartan (7.1% to 5.4%) prevented endothelial dysfunction induced by an oral fat load, although the protective effect of quinapril appeared to be more profound. The response to the endothelium-independent vasodilator nitroglycerine was unaltered throughout the study.
CONCLUSIONS
Both losartan and quinapril prevent endothelial dysfunction induced by triglyceride-rich lipoproteins in healthy volunteers. However, the protective effect of quinapril is more pronounced.
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Abbreviations and Acronyms
| | ACE | = angiotensin-converting enzyme | | FMD | = flow-mediated dilation | | LDL | = low density lipoprotein | | NO | = nitric oxide | | NTG | = Nitroglycerin induced dilation |
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